The present invention generally relates to a device for preventing tachyarrhythmias of the human heart. The present invention more particularly relates to such a device which prevents tachyarrhythmias in a human heart which has arrhythmogenic tissue and more particularly, a site or region of myocardial infarction.
Myocardial infarction has long been directly associated with tachyarrhythmias of the human heart such as, ventricular tachyarrhythmias. Myocardial infarctions are areas of dying or dead heart muscle tissue resulting from obstruction of the blood vessels normally supplying blood to the site or region of an infarct. These infarctions create tissue beds which contain regions of tissues which do not die and are a substrate for the existence of re-entrant arrhythmias such as ventricular tachycardia. These surviving arrhythmogenic tissues can be on the epicardium, the endocardium, or both. Once this substrate has been formed by an infarction, an arrhythmia such as ventricular tachycardia can be initiated by heart activity such as a premature ventricular contraction.
It has been shown that premature stimuli can induce sustained re-entrant ventricular tachycardia in an animal model of chronic, transmural infarction. The recovery of refractoriness as well as the patterns of activation were mapped during the initiation and maintenance of sustained monomorphic ventricular tachycardia. In this model, re-entry paths were shown to be present in the surviving tissue on the epicardium.
Electrophysiological testing in patients with a history of myocardial infarction has demonstrated that they may also have this substrate of vulnerability to ventricular tachycardia. In these patients, a catheter is typically advanced down a vein or artery until it is inside one of the ventricles of the heart. A train of electrical stimuli or pulses are then applied to the heart through this catheter. These are applied at fixed intervals such as 300 milliseconds. Following the last of the stimuli, a premature stimulus is applied at a shorter interval. This process is repeated at progressively shorter (premature) intervals until ventricular tachycardia is induced or until the premature stimulus nor longer captures the heart. Such electrophysiological testing thus elucidates the substrate that is susceptible to the induction of ventricular tachycardia.
One device has been proposed for preventing ventricular tachycardia in U.S. Pat. No. 3,937,226. The device described in that patent includes a plurality of electrodes which are placed at selected points on a heart. The plurality of electrodes are paced in response to the sensing of an activation or an R Wave on any of the electrodes. In a second embodiment described in this patent, separate pluralities of sensing and stimulation electrodes are used. As a result of this device operation, the disparity of activation and therefore recovery of the tissues in the various regions near the electrodes were made more uniform. However, this device requires a large number of electrodes and the placement of the electrodes was not based on measured activations, the existence of an infarct site or region, or the location of such an infarct site or region.
A similar system is also described in U.S. Pat. No. 4,088,140. As described in this patent, this system provides pacing either to the plurality of electrodes when a premature activation is sensed on any one of the electrodes or to less than all of the electrodes when an escape interval is exceeded since the last sensing of an R Wave. This system serves to make the activation and the resultant refractoriness more uniform for premature beats or premature ventricular contractions but does not effect the myocardial infarction substrate from beats at normal intervals.
Neither of the above mentioned systems focused on the relationship between the size and location of a myocardial infarction and the propensity for induction o ventricular tachycardia due to a myocardial infarction. As a result, there is a need in the art for an improved implantable device and method for preventing tachyarrhythmias of a human heart which has arrhythmogenic tissue such as a myocardial infarction.